GENERAL DISCUSSION 



Fertility: Intracellular Recovery 



BACQ: I thought that it would be better to concentrate on certain of the points which 

 cover most of the facts and systems that have been discussed in this meeting. First I 

 should hke to have a brief discussion on fertility because we have had no possibiHty yet 

 of discussing Dr. RusseU's paper, and I would like to start the discussion in this way. In 

 the female mouse where the effect of protection is so marked and where there is no 

 division of the cells we have a very good instance of cell recovery; an instance of the 

 capacity of even a very radio-sensitive cell to recover, provided that not too large a 

 smgle dose is given. Could Dr. Russell tell us if this, in his opinion, is comparable to the 

 reduction in the frequency of induced mutations with decrease in dose-rate which he has 

 shown so beautifully? 



RUSSELL: Well, I think we should be very cautious about comparing one kind of recovery 

 with another; the recovery from damage leading to cell death may not be similar to 

 recovery from what is probably pre-mutational damage. We beheve that the dose-rate 

 effect on mutation does represent recovery from pre-mutational damage. It seems unlikely 

 that one can have reversal of the completed mutation. And since the dose-rate effect does 

 indicate recovery of some sort, we conclude that it is probably recovery from pre- 

 mutational damage. But whether there is any biochemical similarity between the recovery 

 from a pre-mutational damage and the recovery from the type of damage that would have 

 led to cell death, I think is just guess-work at the present time. It is, however, interesting 

 that in new data that we hope to get out soon on mutation frequency m oocytes, it still 

 looks as though the dose-rate effect is much greater than in spermatogonia. In other words 

 as we go from a liigh to a low dose-rate there is an even greater depression in mutation 

 rate than was found in spermatogonia. So there is at least some correlation between the 

 apparently marked rate of cell recovery that you so rightly pointed out for the oocytes 

 and the rather large dose-rate effect for mutations. Perhaps these cells do have some 

 remarkably good capacity for recovery that can express itself in both systems. 

 mole: I would lilve to ask why the word recovery is used. Why don't we just say there's 

 less damage? This seems to me to be of quite fundamental importance, because when we 

 use the word "recovery" we tliink of some biological process, and when we say less 

 damage we mean less phj^sical damage in the first instance. 



BACQ: Yes, but one might tliink that in a cell there are two processes in competition, one, 

 the normal capacity for recovery of every cell and the other, the rate of mjury. If the rate 

 of injury is not too great then you've a long time for the recovery capacity to express 

 itself. 



UPTON: This point that Dr. Mole raises is one wloich bothered me for a long time, too. It 

 is tliis: one could distinguish, I tliinlc, between injury as such and recovery from that 

 injury, and at a low dose-rate one might have less injury, not merely more recovery. But 

 I wonder whether this isn't a semantic question now, in that if one has the same number of 

 ionization events from a given total dose of radiation, then one is looking at the effect of 

 that number of ionization events. One must repair injury at the ionization level, even 

 though tliis is never expressed in terms of any biologically detectable injury. 

 ALEXANDER: This is really the same point. If we consider that the primary injury is a 

 chemical reaction, and we have every reason for beheving this to be the case, then we 

 know of almost no chemical reactions that are highly dose-rate dependent except for 



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